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PubMed1988

Gastritis--a misused term in clinical gastroenterology.

Gastritis is an inflammation in the gastric mucosa. The definition, classification and diagnosis of gastritis is based on morphological changes. The term 'gastritis' is widely used as a catchbag for upper abdominal complaints. Although acute or specific forms of gastritis may present upper abdominal symptoms, chronic gastritis is asymptomatic, and is not the cause of long standing upper abdominal complaints. Chronic gastritis is a very common condition in the general population. Hence the probability of finding chronic gastritis in endoscopic biopsies of patients with upper abdominal complaints is high for statistical reasons, and this does not prove any causal relation between chronic gastritis and subjective complaints. Campylobacter pylori is associated with chronic gastritis. It may activate the inflammatory process in the gastric mucosa, or it may just be an innocent bystander, which subsists within a diseased mucosa. The role of campylobacter pylory in the etiology of non-ulcer dyspepsia or peptic ulcer is questionable.

Adult↗
PubMed1989

Pathogenicity of Campylobacter pylori--a causative factor in gastritis?

There is now much worldwide evidence that Campylobacter pylori plays a pathogenic role in the aetiology of gastritis rather than colonizing an already inflamed gastric mucosa. 1) There is a very close association between the presence of C. pylori on the gastric mucosa and histologically confirmed Type B chronic active gastritis. Ninety percent of patients with C. pylori infection have gastritis whereas less than 5% of patients with normal mucosa are colonized. 2) C. pylori only colonizes gastric type mucosa; it is not found colonizing intestinal type mucosa in the stomach. 3) Two volunteer studies have confirmed Koch's third and fourth postulates. Ingestion of C. pylori led to the development of histologically proven gastritis. 4) Outbreaks of hypochlorhydric C. pylori gastritis have occurred. In one such epidemic 17 of 37 volunteers developed C. pylori hypochlorhydric gastritis after acid secretion studies were undertaken with an unsterilized pH electrode. 5) Susceptible animal models (gnotobiotic piglets and the macacus monkey) inoculated with a suspension of C. pylori have developed histologically proven gastritis. 6) Clearance of C. pylori with antimicrobial agents (amoxicillin or nitrofurantoin) or bismuth salts (colloidal bismuth subcitrate or bismuth salicylate), alone or in combination, leads to rapid resolution of the histologically confirmed gastritis. If relapse occurs the gastritis returns.

Animals↗
PubMed2005

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients.

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.

Adolescent↗
PubMed1999

[Changes in Helicobacter pylori gastritis caused by therapy with inhibitors of gastric acid secretion].

UNLABELLED: In patients with Helicobacter pylori (Hp) gastritis long-term treatment with omeprazole leads to a worsening of the corpus gastritis. In the present overview we have analyzed the literature and our own studies to determine whether this also applies to other proton pump inhibitors (PPI), H2-receptor antagonists (H2-RA) and antacids. RESULTS: Every antisecretory therapy--vagotomy, antacids, H2-RA and PPI--in patients with Hp gastritis leads to a worsening of the following parameters: Grade of gastritis, activity of gastritis, grade of replacement of foveolar epithelium by regenerative epithelium and grade of mucus depletion. The incidence of intestinal metaplasia does not increase. Atrophic gastritis has not been observed after one year of treatment; after five years of treatment with PPI, development of atrophy is uncertain. In the antrum treatment with PPI, but not with antacids or H2-RA, leads to an improvement in the gastritis parameters. The question whether the aggravation of corpus gastritis under antisecretory treatment might be detrimental over the long-term, whether, for example, the more pronounced gastritis might increase the risk of a subsequent carcinoma, remains to be clarified by long-term studies.

Antacids↗
PubMed1998

Helicobacter pylori infection and erosive gastritis.

One hundred and eleven patients were included in the study. Thirty seven had erosive gastritis, thirty four chronic gastritis and forty were controls without any gastrointestinal diseases confirmed by symptoms and upper gastrointestinal endoscopy. Patients with erosive gastritis were divided into non-steroidal anti-inflammatory drug (NSAID) users and non-users. H pylori status was determined by urease test, serology and/or histology. The prevalence of H pylori was compared between the various groups. The prevalence of H pylori infection in erosive gastritis, chronic gastritis and controls was 68%, 76% and 65%, respectively, the difference was not significant (P > 0.05), 8 out of 11 patients with erosive gastritis and NSAID use (73%) were positive for H pylori. Likewise 17/26 patients with erosive gastritis without NSAID use (65%) were positive for H pylori (P > 0.05). Body of the stomach (65%) was the commonest site for erosions compared to antrum (43%) or fundus (27%) (P < 0.02). H pylori infection does not predispose to erosive gastritis. NSAID use does not affect H pylori prevalence. Routine H pylori eradication is, therefore, not indicated in patients with erosive gastritis infection. Body of the stomach is the most predominant site for erosions.

Adult↗
PubMedDate not supplied

[Histopathological findings in nodular gastritis. Experience at the Cayetano Heredia National Hospital ].

INTRODUCTION: Nodular gastritis is a frequent endoscopic finding at our hospital, of 3600 upper endoscopies done from 1994 to 1997, 261 presented with this endoscopic characteristic. The aim of this study is to find whether there is any particular histopathological pattern in nodular gastritis. MATERIAL AND METHODS: 112 gastric biopsies of patients with an endoscopic diagnosis of nodular gastritis were compared to a control group of 111 gastric biopsies of patients with the same age and sex but without this endoscopic finding of nodular gastritis. Patients with peptic ulcer, duodenitis and neoplasia were excluded. Biopsies were blindly reviewed by one experienced pathologist. The following parameters were considered: presence and type of gastritis, grade of mucosal inflammation, presence and percentage of complete or incomplete metaplasia, presence and grade of inflammatory activity, presence and number of lymphoid follicles (primary and secondary), presence and number of eosinophils in the mucosa, presence of H. pylori and presence of epithelial edema. RESULTS: Patients with nodular gastritis were constituted by 62 women and 50 men, the control group by 62 women and 49 men. The average age for the nodular gastritis group was 37 + 17 years (16-82 years) and the control group 38+17 years ( 16-82 years). Both groups had the same number of lymphoid follicles (primary and secondary). Statistical differences were found in relation to : grade of mucosal inflammation (p: 0.042), presence of superficial eosinophils on the surface (p: 0.019) and presence of Helicobacter pylori (p: 0.024). CONCLUSIONS: Nodular gastritis is a chronic gastritis with superficial eosinophilic infiltration, moderate inflammation and an important inflammatory activity associated with the presence of H. pylori. There is no relation with the presence and number of lymphoid follicles. The nodular pattern seen on endoscopy could be related to inflammation mediated by the eosinophil and probably induced by H.pylori or other factors as infectious agents, environment, nutritional, or other individual factors not considered in this study.

Adolescent↗
PubMedDate not supplied

Accumulation of mast cells and macrophages in focal active gastritis of patients with Crohn's disease.

BACKGROUND/AIMS: Recent studies have shown that focal active gastritis seems to be the typical gastric pathology in Crohn's disease. The aim of this study was to compare the incidence of focal active gastritis, Helicobacter pylori infection and distribution of gastric mast cells and macrophages in patients with Crohn's disease, ulcerative colitis and H. pylori gastritis without inflammatory bowel disease. METHODOLOGY: Patients with histologically confirmed Crohn's disease (n = 25) or ulcerative colitis (n = 25) and control patients without inflammatory bowel disease (n = 25) were included in this study. Biopsy specimens were obtained from the antrum and corpus of each patient, and stained with hematoxylin and eosin and immunostained using antibodies to tryptase (AA1) and CD68. The number of mast cells and macrophages located in the lamina propria was determined. RESULTS: Focal active gastritis was detected in 54% of H. pylori-negative patients with Crohn's disease, but it was not found in patients with ulcerative colitis nor in the control group. The density of mast cells and macrophages in the lamina propria of H. pylori-positive patients was significantly higher than in H. pylori-negative patients in all groups. In the Crohn's disease group, the number of mast cells (antrum; 83 +/- 11, body; 89 +/- 11/mm2) and macrophages (antrum; 94 +/- 22, body; 92 +/- 17/mm2) in the lamina propria of H. pylori-negative patients with focal active gastritis was halfway between that in H. pylori-positive and H. pylori-negative patients. In focal active gastritis, mast cells accumulated at the border of focal active gastritis, whereas macrophages accumulated in the center of such lesions. CONCLUSIONS: Our findings indicated that the diagnosis of focal active gastritis, using immunostain for mast cells and macrophages, is the histological hallmark of gastric Crohn's disease. Macrophages might be associated with the formation of focal active gastritis in patients with Crohn's disease.

Adult↗
PubMed2002

Helicobacter pylori and different topographic types of gastritis: treatment response after successful eradication therapy in functional dyspepsia.

BACKGROUND: Helicobacter pylori gastritis is usually a lifelong disease which can cause different topographical inflammatory reactions and induce divergent effects on acid secretion in humans. High acid output and antrum-predominant gastritis are associated with duodenal ulcer disease, whereas corpus-predominat gastritis has been associated with low acid output and risk of gastric carcinoma. The objective of this study was to evaluate the role of different gastritis subtypes in the long-term treatment response of H. pylori-positive functional dyspepsia. METHODS: The gastric biopsies from 143 H. pylori-positive patients with functional dyspepsia were classified in accordance with the Sydney System as antrum-predominant gastritis, pangastritis or corpus-predominant gastritis. The patients were randomized to receive either eradication therapy or placebo antibiotics. Moreover, to standardize acid suppression every patient received omeprazole therapy for the first 3 months. Dyspeptic symptoms were evaluated from a questionnaire and the follow-up time was 12 months. In addition, delta-over-baseline (DOB) values of the 13C-urea breath test (UBT) were analysed from a subgroup of 36 patients to measure urease activity of the stomach. RESULTS: After 1 year, the dyspepsia symptom score was 7.4 +/- 3.0 (95% CI 6.6-8.2) in successfully H. pylori-eradicated patients and 7.6 +/- 3.1 (95% CI 6.9-8.4) in controls (P = ns). Among patients with antrum-predominant gastritis, dyspepsia score was reduced more in subjects whose H. pylori was eradicated than in controls with ongoing infection (-3.6 +/- 2.9 versus -1.7 +/- 2.9; P = 0.05). High urease activity of the stomach was associated with severe or moderate chronic antrum-predominant gastritis. CONCLUSIONS: Patients with antrum-predominant H. pylori-positive chronic gastritis and functional dyspepsia get symptom improvement after successful eradication therapy. A high DOB value of UBT is associated with these patients.

Amoxicillin↗
PubMed1992

Active autoimmune gastritis without total atrophy of the glands.

To date, autoimmune gastritis has been diagnosed for the most part only when total atrophy of the oxyntic glands is detected. On the basis of 40 patients without total atrophy of the glands, and with parietal cell antibodies in the serum, we show that the diagnosis of type A gastritis is also possible in the pre-atrophic stage. The histological criteria for the diagnosis of active autoimmune gastritis without total atrophy of the glands are 1. usually dense, diffuse locally emphasized lymphocytic infiltration of the lamina propria between the glands in the oxyntic mucosa, 2. focal destruction of individual glands in the corpus of the stomach by lymphocytes, and 3. reactive pseudohypertrophy of the parietal cells. A comparison with a group of patients with autoimmune gastritis and total atrophy of the glands shows that in active autoimmune gastritis, too, women are more frequently affected than men (in both groups, the sex ratio is approximately 3:1). Patients without atrophy of the glands are, on average, about 12 years younger than those with "burnt out" type A gastritis (average age 69.98:57.80 years). While in the case of burnt out type A gastritis, no colonisation with Helicobacter pylori was to be found, such colonisation was demonstrated for the corpus mucosa in 22.5%, and for the antral mucosa in 15.0%. In 27.5% a minimal or low-grade inactive superficial gastritis, as may be seen after eradication of Helicobacter pylori, was additionally diagnosed in the antrum. A knowledge of the histological appearance of the pre-atrophic stage of type A gastritis might be of importance for the possible prevention of pernicious anaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

[Expression of gastrin, somatostatin, PCNA and Fas-L in the mucosa of gastric antrum of children with chronic gastritis and duodenal ulcer].

OBJECTIVE: Since application of pediatric gastroscopy in the mid-nineteen nineties, there has been a trend that the prevalence rates of pediatric gastritis and duodenal ulcer (DU) are increasing. The diagnosed rate of pediatric gastritis has accounted for 85% - 95% of the total number of children who received gastroscopy, and the rate of DU accounted for 8% - 22%. Such a high rates of the diseases may influence the development of the children severely. However, the etiology and pathogenesis of pediatric chronic gastritis and DU have not been completely elucidated. The disordered gastrointestinal hormones play a crucial role in the pediatric chronic gastritis and DU. This study focused on the expression of gastrin (GAS), somatostatin (SS) in the mucosa of gastric antrum and PCNA and Fas-L in the sinus ventriculi and their possible roles in the pathogenesis of pediatric chronic gastritis and DU. METHOD: The sinus ventriculi mucosal samples of 83 cases were collected via gastroscopic biopsy from the hospital during the recent two years and the cases were divided into five groups: group A, chronic superficial gastritis, Helicobacter pylori (Hp)(+); group B, chronic superficial gastritis, Hp(-); group C, DU, Hp(+); Group D, DU, Hp(-); Group E, normal sinus ventriculi mucosa, Hp(-). Immunohistochemical staining (En Vision) was carried out for GAS, SS, PCNA and Fas-L, and positive cells of each slide were counted (x 400). Statistically significant differences among groups for continuous data were assessed with the software SPSS10.0. RESULTS: The expressions of GAS and SS in the groups A through E had no significant difference. The expression of PCNA in group A was significantly higher than that in group B (P < 0.05), and no significant differences were found among the other groups. There were no significant differences in expressions of Fas-L among the five groups. CONCLUSION: There seems to be an increasing tendency in the expressions of GAS and SS in children with chronic gastritis and duodenal ulcer. Hp infection promotes the multiplication of the sinus ventriculi mucosal epithelium cells in the pediatric chronic gastritis.

Adolescent↗
PubMed1988

Gastritis and Campylobacter pylori in healthy, asymptomatic volunteers.

A high prevalence of histologic gastritis in asymptomatic individuals has been reported in the literature. The studies have been poorly controlled for gastritis risk factors. We evaluated 20 healthy, asymptomatic volunteers free of known risk factors for gastritis with endoscopy, mucosal biopsy, culture, and gastric pH determination. The prevalence of gastritis on histologic examination was found to be 20%. There was no relationship between the presence of macroscopic findings at endoscopy and the presence of histologic gastritis. In all instances where histologic gastritis was documented, Campylobacter pylori was observed in the gastric mucus. Mucosal tissue invasion by C pylori was not observed. The presence of gastritis and C pylori was associated with fasting hypochlorhydria. Follow-up evaluation was performed eight to 13 months after the initial endoscopic evaluation in three of the volunteers with positive test results. Persistence of C pylori and gastritis was observed. These findings suggest that histologic gastritis is common in healthy, asymptomatic individuals and is strongly associated with the presence of C pylori.

Adult↗
PubMed1983

[Autoimmunity factor in chronic gastritis: incidence of antiparietal cell antibodies and their relation to antral histology and basal blood gastrins].

In 118 patients with histological proven chronic gastritis, was performed a study of seric antibodies against parietal cells (ACCP), following the indirect inmuno-fluorescence method. The results were positives in 36 cases (30%). Four positives cases were found in 40 normal controls (10%), two of them were compensated diabetics, one have the thyrohyoid Hashimoto's disease, and the remainder, brother of a patient with chronic gastritis, was a positive ACCP. A major positiveness (44.4%) was obtained in 9 cases of gastric atrophy than in 65 cases with atrophic gastritis (32%) and in 44 cases of superficial gastritis (25%); although due to the few cases of gastric atrophy regarding other histological types, conclusions cannot be obtained about the incidence of ACCP and histological variety of chronic gastritis. If we do group the patients according to their acid secretory debit, 53 achlorhydric patients had a positiveness of ACCP of 45%, while over 63 with decreased secretory capability, only 18.4%, was positive. The distribution by age groups, shows a major incidence of ACCP about the 4th and 5th decade of life. Thirty seven patients with chronic atrophic gastritis and achlorhydria, and seven with chronic superficial gastritis and hypochlorhydria, besides the antibodies study were on a basal dosage of gastrinemia and antral endoscopic biopsy, finding out that, achlorhydric patients (15 on 19) with normal or slightly altered antrus, have gastrinemia (222 +/- 123 Pgo/oo) and the majority of patients with normal gastrinemia (32 +/- 16 pgo/oo) have more important antral lesions. The ratio between antral histology and ACCP in auto--immune gastritis (Type A), conciliates only partially with the observation by Strickland et al., as only 52.4% of achlorhydric patients and ACCP have a normal antrus or al least with mild lesions. Our results suggest the possibility of that on auto--immune gastritis could act other pathogenic factors of antral lesion.

Adult↗
PubMed1996

Etiological involvement of Helicobacter pylori in "reflux" gastritis after gastrectomy.

OBJECTIVES: "Reflux" gastritis after gastrectomy is associated with various symptoms that are often detrimental to the patients' quality of life. However, prevention of the reflux does not always bring relief from the symptoms of gastritis. Helicobacter pylori (H. pylori) is now considered one of the most important pathogenetic factors in gastritis. The association between H. pylori infection and reflux gastritis after gastrectomy was investigated in the present study. METHODS: In total, 115 patients who had undergone gastrectomy were entered in this study. Five biopsy specimens from the gastric remnant were taken during upper GI endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. The histological degree of gastritis was determined according to the score system of Rauws et al. RESULTS: Forty-six patients (40%) demonstrated H. pylori infection in their stomachs. The prevalence of the infection was significantly higher in patients with conventional gastrectomy than in those with subtotal gastrectomy. The prevalence of H. pylori infection was significantly lower in patients who had undergone gastrectomy more than 4 yr ago. The histological gastritis score in patients with H. pylori infection was significantly higher than in those without H. pylori infection. Furthermore, the eradication of H. pylori in patients with both serious gastritis symptoms and no bile reflux improved the symptoms and significantly decreased the histological gastritis score. CONCLUSIONS: The results suggest that H. pylori is a factor in the pathogenesis of reflux gastritis after gastrectomy.

Amoxicillin↗
PubMed1997

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia.

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.

Atrophy↗
PubMed1983

Course of antrum and body gastritis in pernicious anemia families.

The course of antrum and body gastritis was studied using an essentially linear multicompartmental model in pernicious anemia probands, their first-degree relatives, and controls consisting of a representative family sample of a large Finnish population. Our earlier dynamic approach showed that progression of body gastritis was virtually identical in a series followed up with biopsies and in cross-comparison analyses, indicating that cross-sectional data can be used for dynamic analyses at a population level. The collected data fitted a model which consisted of stepwise progression of body gastritis to severe atrophy, of corresponding progressive steps for antral gastritis, and of regression of the antral changes after the end-stage of the body process had been reached. In addition, acceleration of the progression of gastritis in older subjects had to be taken into account in the model construction. The main findings which characterized pernicious anemia probands and their close relatives were: (1) a rapid overall progression of body gastritis particularly after 50 years of age; (2) a very rapid progression of body atrophy in its final stages, which was unrelated to age; (3) the occurrence of juvenile severe body atrophy; and (4) the healing of antral gastritis which was most marked at the stage of superficial gastritis. These results may offer a dynamic explantation for the occurrence of severe body atrophy in association with a normal or slightly altered antral mucosa in pernicious anemia and the prepernicious anemia state.

Adult↗
PubMed1984

Age-related trends of gastritis and intestinal metaplasia in gastric carcinoma patients and in controls representing the population at large.

Age-related trends of gastritis and intestinal metaplasia (IM) were studied in 476 endoscopically examined and bioptically proved cases of gastric carcinoma (GC), 263 of which were of intestinal (IGC) and 213 of diffuse (DGC) types. Endoscopic biopsy specimens from the area around the tumour were available in all cases, and from the antrum and/or body distant from the tumour area in 238 cases. A representative sample of an endoscopically and bioptically examined Finnish population consisting of 431 subjects was used as control material. In patients with IGC the prevalence of atrophic gastritis in the gastric area affected by the tumour was higher and that of superficial gastritis lower than expected, and the age-group scores of gastritis and IM were situated above the age-dependent line of gastritis scores of controls in all age groups studied. This was seen to indicate a more rapid progression of gastritis in IGC patients than in the population at large. In the opposite area of the stomach, i.e. in the tumour-free area, the progression of gastritis and IM was virtually similar to that in controls. No such differences were seen with regard to DGC. It is concluded that IGC is dynamically closely linked to gastritis and IM, while in DGC no such relationship is demonstrable.

Adenocarcinoma↗
PubMed2002

[Morphology of gastritis and Helicobacter pylori infection].

Helicobacter pylori infection almost invariably results in chronic gastritis. The Sydney System (1990) emphasised the importance of combining topographical, morphological and etiological aspects in attempt to make clinical useful diagnosis of chronic gastritis. The aims of revised Sydney System in Houston (1994), Texas, were to improve terminology of chronic gastritis emphasising distinction between nonatrophic and atrophic gastritis, and in addition to determinate special forms of gastritis. The special forms of gastritis were described and diagnostic criteria were provided. Principles and grading of histological division of Sydney System were only slightly modified, grading being improved by the provision of a visual scale. Endoscopy and histological findings of 1062 patients from University Hospital Merkur were compared to evaluate the value of endoscopic division of Sydney System, and the modified grading proposed by Houston classification. There was no correlation between endoscopic and histological findings. Localisation of inflammatory cells was either 1) superficial or 2) diffuse in the mucosa, respectively. In Helicobacter pylori positive patients the most common finding was chronic active gastritis, and in Helicobacter pylori negative superficial and inactive chronic gastritis.

Biopsy, Needle↗
PubMed1991

[Chronic gastritis and Helicobacter pylori infection on the Ivory Coast. A series of 277 symptomatic patients].

Only a few reports have established the importance of chronic gastritis and Helicobacter pylori infection in Africa. The aim of this study was to ascertain the prevalence of chronic gastritis and Helicobacter pylori infection in a symptomatic population in Abidjan, Côte-d'Ivoire. The study included 277 consecutive patients referred for gastroscopy. Two hundred nine patients complained of abdominal pain without gastroduodenal ulcer or cancer: 26 had a duodenal ulcer, 23 had a gastric ulcer, and 6 had gastric cancer. The remaining 14 patients underwent gastroscopy for various other reasons. Chronic gastritis was present in 89 percent of cases, of which 96 percent showed signs of activity. There were four cases of lymphocytic gastritis. Patients with antral chronic gastritis were older (39.43 +/- 14.3 years) than those with normal antral mucosa (33.7 +/- 12 years, P less than 0.05). Helicobacter pylori was present in 91.3 percent of cases, representing all patients with active chronic gastritis, and 60 percent of the patients with normal gastric mucosa. Chronic gastritis was present in 86 percent of patients with abdominal pain, in 100 percent of those with duodenal of gastric ulcer, and Helicobacter pylori were observed in 90, 100, and 91 percent of the same patient groups, respectively. This study demonstrates the high prevalence of chronic gastritis and the very high level of Helicobacter pylori infection in Ivorian patients complaining of various gastrointestinal symptoms. The usefulness and feasibility of therapeutic trials still have to be investigated.

Adolescent↗